Blood - Exam 1

Blood Transport

oxygen and nutrient delivery to tissues, waste removal from tissues, and hormone delivery to target organs

Blood Maintenance

controls body temperature, pH, and fluid volume

Blood Protection

causes blood clotting and prevents infection

Blood

scarlet to dark red in color - darker has less oxygen

5.25 L total volume

7.35 - 7.45 pH range

viscous (thicker) due to erythrocytes (blood cells)

Plasma

fluid (non-living) portion of the blood

90% water with 6 solutes

1. electrolytes - found in greatest number

2. nitrogenous substances (urea, uric acids)

3. organic nutrients (glucose, amino acids, triglycerides)

4. respiratory gases

5. hormones

6. plasma proteins

Plasma Proteins

makes up most of the mass of plasma

most produced by the liver

ex: albumin, fibrinogen, and globulins

Albumin

major transport protein of blood and contributes to water content in blood

if not present water content in blood would lower bc water would follow a solute outside the blood

Fibrinogen

soluble protein that functions in blood clotting

Globulins

transport proteins and antibodies (immune defense)

Blood Cells

all are short lived and non-mitotic (don’t divide)

3 types

1. erythrocytes (RBC)

2. leukocytes (WBC)

3. thrombocytes (platelets)

Hematocrit

portion of total blood volume made up by erythrocytes

male - 47%

female - 42%

Hematopoiesis

production of blood cells (all 3 types) in red bone marrow

Hematopoietic Stem Cells

aka. hemocytoblast

what all blood cells arise from

start undifferentiated and become committed to forming a certain type of blood cell, once committed the cell cannot become any other cell type

red marrow produces billions of new cells a day

Erythrocytes RBC

blood cell type responsible for respiratory gas transport

nuclei and organelles removed during cell development - creates more space for hemoglobin and oxygen

contains hemoglobin

large surface area relative to volume = increases exchange with less space to cross

flattened disc shape = increases exchange with less distance for O2 to cross

anaerobic mechanism of energy = increases exchange bc they donate 100% of the oxygen they hold and don’t use any

Hemoglobin

protein responsible for O2 transport in blood - found in RBC

composed of a heme pigment bound to a globin protein

each can bind to and carry 4 oxygen molecules

binds and breaks free of oxygen easily - gives body easy access to oxygen

Globin

made up of 2 alpha chains and 2 beta chains

each chain binds to 1 heme group

4 chains total, 4 heme groups, 4 Fe, and 4 O2 molecules carried

Heme

each has an Fe+ ion at the center

each Fe+ can bind to one oxygen molecule

Erythropoiesis

the production of red blood cells

hematopoietic stem cell commits to a proerythroblast

strictly regulated process - too few has not enough HB or oxygen and too many causes thick blood which forces heart to work too hard

RBC Stem Cell

hematopoietic stem cell - hemocytoblast

RBC Committed

proerythroblast

Erythropoietin EPO

directly stimulates erythrocyte production

produced and released by kidneys

only stimulates cells already committed to becoming erythrocytes

small amounts always present in blood to set basal production rate

increased by hypoxic or anemic conditions

negative feedback - excessive oxygen suppresses release

Testosterone

enhances production of EPO

males generally have more erythrocytes and HB than females

Erythrocyte Nutrients

amino acids, lipids, carbohydrates for cell synthesis

B Complex Vitamins

needed for erythrocyte production

B12 and folic acid - necessary for normal DNA synthesis

Iron

needed for erythrocyte production

65% of body’s supply is in HB

remainder stored in liver and spleen

free molecules bound to the protein transferrin - erythrocyte takes in as needed

Destroying Erythrocytes

120 day average lifespan

over time HB degenerates and RBC becomes less flexible

macrophages engulf and destroy cell and heme splits free from globin

globin proteins are broken down to amino acids and released to circulation

Fe2+ is saved for reuse

Bilirubin

substance in the liver consisting of broken down heme groups

excreted to the intestine and released in feces

Transferrin

protein that free iron binds to

erythrocyte takes up iron as needed

Anemia

insufficient oxygen supply to meet body’s needs

symptoms: paleness, cold, short of breath, and tired

caused by blood loss, inadequate erythrocyte production (iron deficiency and renal - no EPO) , and excessive erythrocyte destruction or deformation (sickle cell)

Acute Hemorrhagic Anemia

severe, swift blood loss

Chronic Hemorrhagic Anemia

slow, persistent blood loss

ex: ulcer bleeding and hemorrhoids

Polycythemia

increase in number of erythrocytes

more RBC causes thicker blood that the heart must beat harder to move

Polycythemia Vera

hematocrit levels - 80%

blood volume doubles, vascular system engorges with blood and impairs circulation

treatment: therapeutic phlebotomy (having blood removed)

Secondary Polycythemia

increased EPO release due to low oxygen availability

caused by high altitude living

Blood Doping

temporary polycythemia caused by synthetic EPO/oxygen carriers or use of blood transfusions

causes risk of stroke or heart failure

Blood Loss Compensation

body decreases blood volume to injured blood vessels and increase RBC production by red bone marrow to conserve blood

losing 15-30% leads to weakness, 30%+ leads to severe shock or death

full transfusions are rare most are RBC transfusions

Antigens

specific extracellular markers found on erythrocytes

transfusions cannot occur if two people have different ones bc the immune system will reject it

medical field is mostly concerned with ABO and Rh groups

Type A

cells have an A antigen

cells have anti B antibodies

Type B

cells have a B antigen

cells have anti A antibodies

Type O

cells have no antigen

cells have both anti A and anti B antibodies

Type AB

cells have both an A and B antigen

cells have no antibodies

Agglutinins

immune system antibodies that will attack mismatched blood cells

Rh Groups

made up of 5 antigens = C, D, E, c, e

Rh + can receive Rh - blood

Rh - can not receive Rh + blood

Rh Positive

D antigen

can receive negative blood

Rh Negative

C, E, c, or e antigens

cannot receive positive blood

Transfusion Reaction

caused by mismatching blood types and antibodies attack the foreign donor blood cells

foreign erythrocytes clump together and clog blood vessels

foreign blood cells start to lyse and release free hemoglobin into the blood stream which decreases oxygen and free hemoglobin causes kidney damage

Agglutination

foreign erythrocytes clumping together and clogging blood vessels

Universal Donor

type O

neither antigen is present so they produce no antigens for the immune system to reject

can only receive type O blood because they create anti A and B antibodies

Universal Recipient

type AB

neither antibody is present because they contain both A and B antigens and the immune system wont fight off foreign cells

they can only donate to other AB types

Leukocytes WBC

responsible for defending the body

not restricted to blood vessels and use them as transport to body parts

can leave vessels via capillary walls to kill pathogens before they enter the bloodstream

can be produced fast within 2-3 hours

average lifespan of 13-20 days

two types: granulocytes and agranulocytes

Granulocytes

spherical in shape, large, and packed with granules

3 groups: neutrophils, eosinophils, and basophils

Neutrophils

bacteria killer

50-70% of total leukocyte population

granules contain defensins

chemically attracted to sites of inflammation

can become phagocytic

Defensins

contained in granules inside neutrophils

an antimicrobial protein that kills off bacteria by punching holes in the membrane

Eosinophils

parasite killer

2-4% of leukocyte population

lysosome in cells contain digestive enzymes

don’t have enzymes that kill bacteria

digestive enzymes released digest body wall of parasitic worms

Basophils

0.5-1% of leukocyte population

have histamine containing granules

Histamine

release causes vasodilation and attracts other leukocytes to the area

more blood to infected areas that WBC can use for transport and positive chemotaxis

Agranulocytes

leukocytes that lack visible granules with a large nucleus

2 types: lymphocytes and monocytes

Lymphocytes

25% of leukocyte population

migrate into and out of the blood continuously

3 types - T lymphocytes, B lymphocytes, and natural killers (NK)

T Lymphocytes

act against virus infected cells and tumor cells

B Lymphocytes

produce antibodies released to blood

Natural Killer

act against virus infected cells and tumor cells

Monocytes

3-8% of leukocyte population

differentiate into macrophages as they leave the bloodstream and enter damaged/infected tissue

actively phagocytic and destroy bacteria, viruses, sources of chronic infection

Leukopoiesis

production of leukocytes

stimulated by interleukins and colony stimulating factors

Leukocyte Differentiation

hematopoietic stem cells can form either myeloid stem cells or lymphoid stem cells

Myeloid Stem Cell

commits to either myeoblast or monoblasts

Lymphoid Stem Cell

commits to either B-lymphocyte or T-lymphocyte precursor cells

Leukemia

cancer resulting in the over production of abnormal leukocytes

extra cells originate from a single abnormal cell

abnormal leukocytes remain unspecialized and proliferate extensively

cancerous leukocytes crowd red marrow and immature leukocytes flood the bloodstream

other blood cell types are crowded out of blood and results in anemia and bleeding problems

do not defend the body as they should - causes infection and hemorrhage

Acute Leukemia

derived from stem cells

primarily affects children

fast development

Chronic Leukemia

derived from later cell stages

primarily affects the elderly

slow development

Myeloid Leukemia

involves myeloid stem cell descendants

Lymphocyte Leukemia

involves lymphocytes

Thrombocytes Platelets

fragments of large megakaryocytic cells

average lifespan - about 10 days if unused (shorter if used)

initiate blood clot formation after damage to blood vessel wall

formation is regulated by thrombopoietin

Megakaryocytes

fragments of large cells

fragment into smaller platelet cells that are released into the blood as thrombocytes

Platelet Damage

platelets will stick together and stick to the site of injury

Platelet No Damage

prostacyclin and nitric oxide prevent platelets from sticking together

important that they don’t stick together to prevent unnecessary blood clots

Hemostasis

the process by which bleeding is stopped after blood vessel rupture occurs

localized response that progresses very quickly

3 steps: vascular spasm, platelet plug formation, and coagulation

Vascular Spasm

rapid constriction of a damaged blood vessel triggered by injured smooth muscle tissue, chemicals released by damaged cells in vessel wall, and reflexed from local pain receptors

smaller vessels prevent large amounts of bleeding and blood loss

Step 2 Platelet Plug Formation

platelets stick together and to fibers in vessel wall to form a plug in a damaged vessel

platelets release the following ADP and serotonin and thromboxane A² in response to injury

only good for general wear and tear and smaller injuries - larger injuries require a more severe way of stopping bleeding (ex: coagulation)

ADP

causes more platelets to stick to the site of injury

Serotonin and Thromboxane A²

increase vascular spasm and platelet aggregation

Coagulation

formation of a true blood clot

mutli-step process

Coagulation Step 1

clotting factors (I-XIII) form prothrombin activator

clotting factors are produced by liver and all clotting factors are needed for coagulation

Coagulation Step 2

prothrombin activator catalyzes conversion of plasma protein prothrombin into active enzyme thrombin

Coagulation Step 3

thrombin catalyzes transformation of clotting factor fibrinogen into fibrin molecules

fibrin molecules link together to form long insoluble strands that stick together

uses factor XIII

fibrin strands also trap platelets and RBCs to form a blood clot

Factor XIII

enzyme that binds fibrin strands to one another to form a strong mesh at damage site that forms blood clot

Blood Clot Retraction

the process of pulling damaged edges of blood vessel close together so there is a smaller area of damage to recover

platelets have contractile ability to pull fibrin strands together and pull edges of injury together

has a platelet derived growth factor

Platelet Derived Growth Factor

causes an increase in number of fibroblasts and smooth muscle cells in damaged area

forms connective tissue that will eventually form new blood vessel wall where damage occured

Fibrinolysis

the removal of a blood clot after healing is complete

if they are left they will build up and block blood flow

uses plasmin

typically within 2 days of clot formation

Plasmin

enzyme that digests fibrin - usually within 2 days

Thromboembolic Disorders

formation of undesired/unnecessary blood clots

ex: thrombus and embolus

Thrombus

formation of blood clot in unbroken vessel - remains stuck to wall

blocks circulation

Embolus

thrombus that breaks free and enters circulation

if small - generally not a problem

if big - can obstruct smaller blood vessels and block circulation

Bleeding Disorders

absence of desirable blood clots leading to excessive bleeding

ex: thrombocytopenia and hemophilia

Thromnocytopenia

low number of platelets in circulation

limited ability of body to form platelet plug - even small breaks can cause massive hemorrhages

caused by anything that decreases red bone marrow that usually decreases platelet count

Hemophilia

hereditary of bleeding disorders

deficiency or absence of certain clotting factors causing extreme bleeding from small cuts or injuries

prolonged bleeding into tissues and painful, disabled joints

treated by plasma transfusions and injections ob absent/deficient clotting factor

Hemophilia A

deficiency of clotting factor VIII

most dangerous

Hemophilia B

deficiency of clotting factor IX

rarest type

Hemophilia C

lack of factor XI

least dangerous